Hypoxic-ischaemic encephalopathy (HIE) remains one of the leading causes of neonatal morbidity and mortality worldwide, occurring due to impaired cerebral oxygenation and blood flow during the perinatal period. Despite significant advances in obstetric care, neonatal resuscitation, and neuroprotective strategies such as therapeutic hypothermia, HIE continues to contribute substantially to long-term neurological disabilities, including cerebral palsy, epilepsy, cognitive impairment, developmental delay, and sensory dysfunction.[1-3] The extent of neurological injury depends on the severity, duration, and timing of the hypoxic-ischaemic insult, with early identification of brain injury being essential for prognostication, parental counselling, and timely initiation of supportive interventions.[4]The pattern of cerebral injury in HIE varies according to the nature of the insult. Acute and severe hypoxic events commonly result in injury to metabolically active deep grey matter structures, particularly the basal ganglia and thalami, and are associated with severe neurological impairment. In contrast, prolonged partial hypoxic insults may produce watershed-pattern injury involving the cerebral cortex and subcortical white matter, which may subsequently manifest as cognitive, behavioural, and developmental deficits. Therefore, accurate assessment of the extent and pattern of brain injury is crucial for predicting neurological outcomes.[5,6]Clinical evaluation remains the cornerstone of early assessment of HIE severity. Neurological scoring systems such as modified Sarnat staging, Thompson score, and neonatal encephalopathy scoring systems assess parameters including consciousness, muscle tone, reflexes, autonomic function, and seizures.[7] These scores are useful for grading encephalopathy severity and guiding therapeutic decisions, including selection of neonates for therapeutic hypothermia.[8] However, clinical assessment may be influenced by factors such as sedative medications, anticonvulsant therapy, observer variability, and the evolving nature of cerebral injury, limiting its ability to accurately reflect underlying structural abnormalities.[9]Magnetic resonance imaging (MRI) is considered the reference standard for evaluating hypoxic-ischaemic brain injury due to its superior ability to detect structural and metabolic changes. Advanced MRI techniques, including diffusion-weighted imaging, apparent diffusion coefficient mapping, magnetic resonance spectroscopy, and perfusion imaging, have demonstrated significant value in predicting neurodevelopmental outcomes.[10] However, routine MRI evaluation in critically ill neonates is often limited due to restricted availability, high cost, and the risks associated with transporting unstable infants.[11]Cranial ultrasound (CUS) provides a practical bedside alternative for early evaluation and serial monitoring of neonatal brain injury. It is widely available, non-invasive, radiation-free, cost-effective, and can be performed repeatedly in critically ill neonates.[12] CUS can identify important abnormalities associated with HIE, including increased cerebral echogenicity, basal ganglia and thalamic abnormalities, cerebral edema, loss of normal brain architecture, ventricular changes, and cystic evolution. Although MRI offers greater sensitivity, CUS remains an important complementary imaging modality, particularly in resource-limited settings.[13]Previous studies have demonstrated associations between abnormal cranial ultrasound findings, higher clinical severity scores, and adverse neurological outcomes. However, the relationship between specific CUS abnormalities, severity grading, and clinical outcomes requires further evaluation to establish its prognostic utility. Integrating cranial ultrasound findings with standardized clinical severity assessment may provide a comprehensive approach for early risk stratification and management planning.[14] Therefore, the present study aims to evaluate the correlation between cranial ultrasound findings, clinical severity scores, and outcomes in neonates with hypoxic-ischaemic encephalopathy

The present study was conducted as a prospective observational study to evaluate the correlation between cranial ultrasound findings, clinical severity scores, and outcomes among neonates with hypoxic-ischaemic encephalopathy (HIE). The study was carried out in the Department of Pediatrics in collaboration with the Department of Radiology at a tertiary care hospital. Study Population The study included 100 neonates diagnosed with hypoxic-ischaemic encephalopathy based on clinical criteria of perinatal asphyxia and neurological examination findings. All enrolled neonates were evaluated clinically for severity of encephalopathy and underwent cranial ultrasound examination for assessment of cerebral abnormalities.A total of 100 neonates with hypoxic-ischaemic encephalopathy were included in the study. The sample size was determined considering the feasibility of recruitment and the availability of eligible neonates during the study period. Study Objectives The study was conducted with the primary objective of evaluating the correlation between cranial ultrasound findings and clinical severity scores in neonates with HIE. The secondary objective was to assess the association of cranial ultrasound abnormalities and severity grading with short-term neonatal outcomes. Inclusion Criteria Neonates were included in the study if they fulfilled the following criteria: Neonates with evidence of perinatal asphyxia and clinical diagnosis of hypoxic-ischaemic encephalopathy. • Term and near-term neonates requiring evaluation for HIE. • Neonates with abnormal neurological findings suggestive of encephalopathy, including altered consciousness, abnormal tone, seizures, or impaired reflexes. • Neonates whose parents or legal guardians provided informed consent for participation. Exclusion Criteria Neonates were excluded if they had: • Major congenital anomalies or chromosomal abnormalities. • Structural brain malformations diagnosed antenatally or postnatally. • Intracranial hemorrhage unrelated to hypoxic-ischaemic injury. • Proven central nervous system infection. • Severe metabolic disorders affecting neurological status. • Incomplete clinical or imaging data. Clinical Assessment and Severity Grading All enrolled neonates underwent detailed clinical evaluation at admission and during the neonatal period. The severity of HIE was assessed using standardized neurological assessment tools, including the modified Sarnat staging system and/or Thompson score. Clinical parameters evaluated included level of consciousness, spontaneous activity, muscle tone, posture, primitive reflexes, autonomic dysfunction, and presence of seizures.Based on clinical assessment, neonates were categorized into mild, moderate, or severe HIE groups according to established severity criteria. Cranial Ultrasound Examination Cranial ultrasound examination was performed using a high-frequency neonatal transducer through the anterior fontanelle. Imaging was conducted during the early neonatal period and repeated when clinically indicated to assess progression or evolution of cerebral abnormalities. The ultrasound evaluation included assessment of: • Cerebral echogenicity and edema. • Basal ganglia and thalamic echogenicity. • Periventricular white matter changes. • Cortical abnormalities. • Ventricular size and configuration. • Loss of normal brain architecture. • Cystic changes or other structural abnormalities. All ultrasound examinations were performed by experienced radiologists/neonatal imaging specialists, and findings were documented. Outcome Assessment Neonatal outcomes were recorded and correlated with clinical severity scores and cranial ultrasound findings. The evaluated outcomes included: • Requirement and duration of respiratory support. • Occurrence of seizures. • Duration of neonatal intensive care unit (NICU) stay. • Need for therapeutic hypothermia, where applicable. • Mortality during hospital admission. • Neurological status at discharge. Data Collection Demographic details, perinatal history, clinical findings, severity scores, cranial ultrasound findings, and neonatal outcomes were collected using a structured data collection proforma. Relevant maternal and birth-related factors, including mode of delivery, gestational age, birth weight, Apgar scores, need for resuscitation, and cord blood parameters (where available), were recorded. Statistical Analysis The collected data were entered into a computerized database and analysed using SPSS .21statistical software. Continuous variables were expressed as mean ± standard deviation or median with interquartile range depending on data distribution. Categorical variables were presented as frequency and percentage. The association between cranial ultrasound findings, clinical severity scores, and neonatal outcomes was analysed using appropriate statistical tests. The correlation between ultrasound parameters and clinical severity scores was assessed using Pearson’s or Spearman’s correlation analysis. The diagnostic and predictive value of cranial ultrasound findings for adverse outcomes was evaluated using receiver operating characteristic (ROC) curve analysis wherever applicable. A p-value of <0.05 was considered statistically significant.

The present study included 100 neonates diagnosed with hypoxic-ischaemic encephalopathy (HIE). The demographic and perinatal characteristics of the study population are presented in Table 1. Among the enrolled neonates, 56% were males and 44% were females. The majority of neonates were born at a gestational age of 37–39 weeks (68%), while 32% were ≥40 weeks. Regarding birth weight, most neonates had a birth weight between 2500–3500 g (72%), followed by low birth weight (<2500 g) in 18% cases. Vaginal delivery was observed in 58% of cases, whereas 42% were delivered by caesarean section. Regarding neonatal resuscitation, positive pressure ventilation was required in 52% of neonates, while 32% required only initial steps of resuscitation and 16% required advanced resuscitative measures (Table 1).Clinical severity grading of HIE according to modified Sarnat staging/Thompson score demonstrated that 46% of neonates had moderate HIE, followed by mild HIE in 34% and severe HIE in 20% of cases. The mean clinical severity score among study participants was 8.6 ± 4.2. The distribution of HIE severity grades is illustrated in Figure 1.Cranial ultrasound evaluation revealed abnormal findings in 62% of neonates, whereas 38% had normal cranial ultrasound examinations. The most common ultrasound abnormality observed was increased cerebral echogenicity (42%), followed by basal ganglia and thalamic abnormalities (28%), periventricular echogenicity (24%), cerebral edema (22%), loss of normal brain architecture (18%), ventricular abnormalities (12%), and cystic changes (8%) (Table 3). The overall distribution of cranial ultrasound findings is represented in Figure 2.The severity of HIE showed a significant association with cranial ultrasound abnormalities. Abnormal cranial ultrasound findings were observed in 35.3% of neonates with mild HIE, 73.9% with moderate HIE, and 80% with severe HIE (p<0.001). Basal ganglia and thalamic abnormalities increased progressively with severity, being present in 11.8% of mild, 30.4% of moderate, and 50% of severe HIE cases (p=0.006). Cerebral edema and increased cerebral echogenicity also demonstrated significant associations with increasing HIE severity (Table 4).Correlation analysis demonstrated a significant positive correlation between cranial ultrasound abnormalities and clinical severity scores. The overall cranial ultrasound abnormality score showed a strong correlation with Thompson score (r=0.68, p<0.001). Basal ganglia/thalamic abnormalities (r=0.52, p<0.001) and cerebral edema (r=0.41, p<0.001) showed moderate positive correlations with severity scores, while increased echogenicity demonstrated a weaker but significant correlation (r=0.36, p=0.002) (Table 5).Neonatal outcomes were significantly associated with cranial ultrasound findings. Neonates with abnormal cranial ultrasound findings had a higher incidence of seizures (51.6% vs 15.8%, p<0.001), requirement of mechanical ventilation (54.8% vs 21.1%, p=0.001), prolonged NICU stay of >14 days (61.3% vs 26.3%, p=0.001), and abnormal neurological examination at discharge (58.1% vs 18.4%, p<0.001) compared with neonates having normal ultrasound findings. Mortality was also higher among neonates with abnormal cranial ultrasound findings (19.4% vs 5.3%, p=0.04) (Table 6). The association between cranial ultrasound abnormalities and neonatal outcomes is depicted in Figure 3. Table 1: Baseline Demographic and Perinatal Characteristics of Study Participants (n=100) Parameter Number (n) Percentage (%) Gender Male 56 56.0 Female 44 44.0 Gestational age 37–39 weeks 68 68.0 ≥40 weeks 32 32.0 Birth weight <2500 g 18 18.0 2500–3500 g 72 72.0 >3500 g 10 10.0 Mode of delivery Vaginal delivery 58 58.0 Caesarean section 42 42.0 Need for resuscitation at birth Initial steps only 32 32.0 Positive pressure ventilation 52 52.0 Advanced resuscitation 16 16.0 Table 2: Clinical Severity Grading of Hypoxic-Ischemic Encephalopathy According to Modified Sarnat/Thompson Score (n=100) Severity of HIE Number (n) Percentage (%) Mild HIE 34 34.0 Moderate HIE 46 46.0 Severe HIE 20 20.0 Mean clinical severity score: 8.6 ± 4.2 Table 3: Cranial Ultrasound Findings Among Neonates with HIE (n=100) Cranial Ultrasound Finding Number (n) Percentage (%) Abnormal ultrasound findings 62 62.0 Normal ultrasound findings 38 38.0 Increased cerebral echogenicity 42 42.0 Basal ganglia and thalamic abnormalities 28 28.0 Periventricular echogenicity 24 24.0 Cerebral edema 22 22.0 Loss of normal brain architecture 18 18.0 Ventricular abnormalities 12 12.0 Cystic changes 8 8.0 Table 4: Correlation Between Cranial Ultrasound Abnormalities and Severity of HIE (n=100) Cranial Ultrasound Finding Mild HIE (n=34) Moderate HIE (n=46) Severe HIE (n=20) p-value Abnormal CUS findings 12 (35.3%) 34 (73.9%) 16 (80.0%) <0.001 Basal ganglia/thalamic changes 4 (11.8%) 14 (30.4%) 10 (50.0%) 0.006 Cerebral edema 5 (14.7%) 10 (21.7%) 7 (35.0%) 0.041 Increased echogenicity 14 (41.2%) 18 (39.1%) 10 (50.0%) 0.018 Statistical test applied: Chi-square test Table 5: Correlation Between Cranial Ultrasound Findings and Clinical Severity Scores (n=100) Parameter Correlation coefficient (r) p-value Overall CUS abnormality score vs Thompson score 0.68 <0.001 Basal ganglia/thalamic changes vs severity score 0.52 <0.001 Cerebral edema vs severity score 0.41 <0.001 Increased echogenicity vs severity score 0.36 0.002 Statistical test applied: Spearman correlation analysis Table 6: Association Between Cranial Ultrasound Findings and Neonatal Outcomes (n=100) Outcome Parameter Normal CUS (n=38) Abnormal CUS (n=62) p-value Seizures, n (%) 6 (15.8%) 32 (51.6%) <0.001 Mechanical ventilation required, n (%) 8 (21.1%) 34 (54.8%) 0.001 Prolonged NICU stay (>14 days), n (%) 10 (26.3%) 38 (61.3%) 0.001 Abnormal neurological examination at discharge, n (%) 7 (18.4%) 36 (58.1%) <0.001 Mortality, n (%) 2 (5.3%) 12 (19.4%) 0.04

Hypoxic-ischaemic encephalopathy (HIE) remains a significant cause of neonatal neurological morbidity and mortality. Early identification of the severity of brain injury is essential for prognostication, parental counselling, and timely management. The present study evaluated the association between cranial ultrasound (CUS) findings, clinical severity scores, and neonatal outcomes among 100 neonates with HIE. The study demonstrated that abnormal CUS findings were significantly associated with increasing severity of encephalopathy and adverse neonatal outcomes, supporting its role as a bedside prognostic tool.In the present study, males constituted 56% of neonates and females 44%. Most neonates were term (37–39 weeks: 68%) with birth weight between 2500–3500 g (72%). Vaginal delivery occurred in 58% cases, and 52% required positive pressure ventilation at birth, reflecting the common association of perinatal compromise and resuscitation requirement with HIE development.Moderate HIE was the most frequent severity category (46%), followed by mild (34%) and severe HIE (20%), with a mean clinical severity score of 8.6 ± 4.2. Although clinical scoring systems such as Sarnat and Thompson scores are widely used for assessment of encephalopathy severity, they primarily represent functional impairment and may not completely reflect underlying structural brain injury.Abnormal cranial ultrasound findings were observed in 62% of neonates. Increased cerebral echogenicity was the most common abnormality (42%), followed by basal ganglia and thalamic abnormalities (28%), periventricular echogenicity (24%), cerebral edema (22%), loss of normal architecture (18%), ventricular abnormalities (12%), and cystic changes (8%). These findings correlate with recognized patterns of hypoxic-ischaemic injury, where severe acute insults predominantly affect metabolically active deep grey matter structures. Tann et al.[15] reported that early CUS could identify characteristic abnormalities involving the basal ganglia, thalami, cortex, and white matter in neonates with HIE.A significant association was observed between CUS abnormalities and HIE severity. Abnormal ultrasound findings were present in 35.3% of mild, 73.9% of moderate, and 80% of severe HIE cases (p<0.001). Basal ganglia and thalamic abnormalities increased progressively with severity, occurring in 11.8%, 30.4%, and 50% of mild, moderate, and severe HIE cases respectively (p=0.006). These findings support previous observations that deep grey matter involvement is associated with severe hypoxic injury and poorer neurological outcomes. Bano et al.[16] described similar injury patterns, emphasizing the prognostic importance of deep grey matter abnormalities. CUS abnormalities showed significant correlation with clinical severity scores. The overall CUS abnormality score demonstrated a strong positive correlation with Thompson score (r=0.68, p<0.001). Basal ganglia/thalamic changes (r=0.52, p<0.001), cerebral edema (r=0.41, p<0.001), and increased echogenicity (r=0.36, p=0.002) were also significantly associated with severity. These findings indicate that CUS provides objective structural information that complements clinical assessment. Although MRI remains the gold standard for HIE evaluation, Wisnowski et al.[17] highlighted the importance of serial imaging in monitoring evolving neonatal brain injury.Abnormal CUS findings were significantly associated with adverse outcomes. Neonates with abnormal CUS had higher rates of seizures (51.6% vs 15.8%, p<0.001), mechanical ventilation requirement (54.8% vs 21.1%, p=0.001), prolonged NICU stay (61.3% vs 26.3%, p=0.001), abnormal neurological examination at discharge (58.1% vs 18.4%, p<0.001), and mortality (19.4% vs 5.3%, p=0.04). Snyder et al.[18] similarly demonstrated that ultrasound-based parameters were associated with severity of brain injury and may assist in early risk stratification.

The present study demonstrated that cranial ultrasound abnormalities were significantly associated with increasing severity of hypoxic-ischaemic encephalopathy and adverse neonatal outcomes. Abnormal CUS findings showed a strong correlation with clinical severity scores and were associated with higher rates of seizures, need for mechanical ventilation, prolonged NICU stay, abnormal neurological examination, and mortality. Cranial ultrasound, being a bedside, non-invasive, and repeatable imaging modality, can serve as a valuable tool for early assessment and prognostication in neonates with HIE. Integration of CUS findings with clinical severity scoring may improve risk stratification and guide timely management decisions. Limitations The study was conducted at a single centre with a relatively limited sample size of 100 neonates, which may affect the generalizability of the findings. Cranial ultrasound assessment was dependent on operator expertise and may have limited sensitivity compared with advanced neuroimaging modalities such as MRI. Long-term neurodevelopmental outcomes were not assessed, and further studies with larger cohorts and extended follow-up are required to validate the prognostic role of cranial ultrasound in HIE

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